基础医学与临床 ›› 2023, Vol. 43 ›› Issue (4): 706-710.doi: 10.16352/j.issn.1001-6325.2023.04.0706

• 短篇综述 • 上一篇    

NLRP3炎性小体在缺血再灌注损伤治疗中作用的研究进展

录亚鹏, 谢建琴*   

  1. 兰州大学第二医院 麻醉科, 甘肃 兰州 730030
  • 收稿日期:2022-01-24 修回日期:2022-05-30 出版日期:2023-04-05 发布日期:2023-04-03
  • 通讯作者: *952456735@qq.com
  • 基金资助:
    兰州大学第二医院“萃英科技创新”(CY2020-MS18)

Research progress on the role of NLRP3 inflammasome in the treatment of ischemia-reperfusion injury

LU Yapeng, XIE Jianqin*   

  1. Department of Anestheiology, the Second Hospital of Lanzhou University, Lanzhou 730030, China
  • Received:2022-01-24 Revised:2022-05-30 Online:2023-04-05 Published:2023-04-03
  • Contact: *952456735@qq.com

摘要: NLRP3 (NLRP3)炎性小体作为组成先天免疫系统的蛋白复合体,可通过调节IL-1β和IL-18的成熟释放介导炎性反应,是机体发生多种病理损伤的基础。缺血/再灌注损伤(I/RI)时产生的多种损伤因子均可激活NLRP3炎性小体,导致IL-1β和IL-18的过度释放,进而引起炎性级联反应使各组织器官的损伤加重。而抑制NLRP3炎性小体活化已成为减轻器官I/RI的有效方法。因此,探究NLRP3炎性小体介导I/RI的详细作用机制,可以为器官I/RI的防治提供理论依据。

关键词: NLRP3炎性小体, 缺血/再灌注损伤, 器官保护

Abstract: NOD-like receptor protein 3(NLRP3) inflammasome, as a protein complex that constitutes the innate immune system, can mediate inflammatory responses by regulating the maturation and release of IL-1β and IL-18, which are the basic for multiple pathological injury. A variety of injury factors generated during ischemia-reperfusion injury (I/RI) can activate the NLRP3 inflammasome, resulting in the excessive release of IL-1β and IL-18, which in turn leads to an inflammatory cascade to aggravate the damage of various tissues and organs. Inhibition of NLRP3 inflammasome activation has become an effective method to alleviate organ I/RI. Therefore, exploring the detailed mechanism of NLRP3 inflammasome-mediated I/RI can provide a theoretical basis for the prevention and treatment of organ I/RI.

Key words: NLRP3 inflammasome, ischemia-reperfusion injury, organ protection

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